The effect of sleep restriction, with or without high-intensity interval exercise, on myofibrillar protein synthesis in healthy young men

被引:39
|
作者
Saner, Nicholas J. [1 ]
Lee, Matthew J. -C. [1 ]
Pitchford, Nathan W. [1 ,4 ]
Kuang, Jujiao [1 ]
Roach, Gregory D. [5 ]
Garnham, Andrew [1 ]
Stokes, Tanner [3 ]
Phillips, Stuart M. [3 ]
Bishop, David J. [1 ,2 ]
Bartlett, Jonathan D. [1 ]
机构
[1] Victoria Univ, Inst Hlth & Sport, Melbourne, Vic, Australia
[2] Edith Cowan Univ, Sch Med & Hlth Sci, Joondalup, Australia
[3] McMaster Univ, Dept Kinesiol, Hamilton, ON, Canada
[4] Univ Tasmania, Sch Human Life Sci, Sport Performance Optimisat Res Team, Launceston, Tas, Australia
[5] Cent Queensland Univ, Appleton Inst Behav Sci, Adelaide, SA, Australia
来源
JOURNAL OF PHYSIOLOGY-LONDON | 2020年 / 598卷 / 08期
基金
加拿大自然科学与工程研究理事会;
关键词
atrophy; high-intensity interval exercise; protein synthesis; sleep loss; SKELETAL-MUSCLE HYPERTROPHY; HUMAN QUADRICEPS MUSCLE; TO-DAY CHANGES; RESISTANCE EXERCISE; DEPRIVATION; TURNOVER; ADAPTATIONS; VALIDATION; BREAKDOWN; RECOVERY;
D O I
10.1113/JP278828
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Key points Sleep restriction has previously been associated with the loss of muscle mass in both human and animal models. The rate of myofibrillar protein synthesis (MyoPS) is a key variable in regulating skeletal muscle mass and can be increased by performing high-intensity interval exercise (HIIE), although the effect of sleep restriction on MyoPS is unknown. In the present study, we demonstrate that participants undergoing a sleep restriction protocol (five nights, with 4 h in bed each night) had lower rates of skeletal muscle MyoPS; however, rates of MyoPS were maintained at control levels by performing HIIE during this period. Our data suggest that the lower rates of MyoPS in the sleep restriction group may contribute to the detrimental effects of sleep loss on muscle mass and that HIIE may be used as an intervention to counteract these effects. The present study aimed to investigate the effect of sleep restriction, with or without high-intensity interval exercise (HIIE), on the potential mechanisms underpinning previously-reported sleep-loss-induced reductions to muscle mass. Twenty-four healthy, young men underwent a protocol consisting of two nights of controlled baseline sleep and a five-night intervention period. Participants were allocated into one of three parallel groups, matched for age, V?O2peak, body mass index and habitual sleep duration; a normal sleep (NS) group [8 h time in bed (TIB) each night], a sleep restriction (SR) group (4 h TIB each night), and a sleep restriction and exercise group (SR+EX, 4 h TIB each night, with three sessions of HIIE). Deuterium oxide was ingested prior to commencing the study and muscle biopsies obtained pre- and post-intervention were used to assess myofibrillar protein synthesis (MyoPS) and molecular markers of protein synthesis and degradation signalling pathways. MyoPS was lower in the SR group [fractional synthetic rate (% day(-1)), mean +/- SD, 1.24 +/- 0.21] compared to both the NS (1.53 +/- 0.09) and SR+EX groups (1.61 +/- 0.14) (P < 0.05). However, there were no changes in the purported regulators of protein synthesis (i.e. p-AKT(ser473) and p-mTOR(ser2448)) and degradation (i.e. Foxo1/3 mRNA and LC3 protein) in any group. These data suggest that MyoPS is acutely reduced by sleep restriction, although MyoPS can be maintained by performing HIIE. These findings may explain the sleep-loss-induced reductions in muscle mass previously reported and also highlight the potential therapeutic benefit of HIIE to maintain myofibrillar remodelling in this context.
引用
收藏
页码:1523 / 1536
页数:14
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